Figure 8.

Hypothetical model of how retrograde signaling may mediate redox communication between endoplasmic reticulum and mitochondria to alleviate reductive stress. A, Thiol-based reductant excess is actively dissipated in mitochondria by flexible uncoupling of respiration from oxidative phosphorylation in WT Arabidopsis plants. The respiratory uncoupling capacity is flexibly upregulated via transcriptional regulation of UCP1 and AOX1a, and via ANAC017-dependent retrograde signaling-controlled AOX1a expression. B, Decreased mitochondrial uncoupling capacity, for example, lack of functional UCP1 or AOX1a, disables efficient dissipation of excess reductant, leading to reducing ER stress. Similarly, perturbation of the retrograde signaling pathway, for example, lack of functional ANAC017, abolishes the efficient upregulation AOX1a expression, thus lowering the dissipation capacity of excess reductant.